lactic acidosis, poisoning with, for example, salicylate, methanol, ethylene
glycol (Chapter 12) or the condition known as inherited organic acidosis all
increase the production of H+. In contrast, a decreased excretion of H+as in
renal tubular acidosis, acute and chronic renal failure (Chapter 8), the use of
inhibitors of carbonic anhydrase or a deficiency of mineralocorticoid, such
as aldosterone (Figure 9.8) all increase blood H+ content. Acid ingestion, as in
acid poisoning, the excessive intake of amino acids by infusion, the direct loss
of HCO 3 – by diarrhea or a pancreatic fistula can all reduce the concentration of
HCO 3 – in the blood.
The clinical effects of metabolic acidosis include hyperventilation, where
the increased H+ concentration acts as a rapid and powerful stimulant of
the respiratory center leading to a deep sighing breathing called Kussmaul
respiration. The patients may also present with neuromuscular irritability that
can cause cardiac arrhythmias. Cardiac arrest is more likely in the presence of
hyperkalemia (Chapters 8 and 14 ). Eventually metabolic acidosis can depress
the activities of the central nervous system and this can progress to coma and
even death. Patients with metabolic acidosis are managed by treating the
underlying cause and this usually resolves the acid–base disorder. In severe
cases, the patients may be administered HCO 3 – intravenously to correct the
acidosis.
Metabolic alkalosis may occur as a consequence of gastrointestinal loss of H+
following vomiting and gastric aspiration or from excessive renal loss of H+ in
Conn’s and Cushing’s syndromes (Chapter 7). Some clinical treatments, such
as the use of carbenoxolone, an anti-inflammatory drug used to treat ulcers,
and thiazide diuretic drugs that reduce blood pressure by promoting the
secretion of urine and by K+ depletion, can also result in this condition. Finally,
the administration of alkali, including alkali ingestion, and inappropriate
treatment for acidosis can also cause metabolic alkalosis.
The clinical effects of metabolic alkalosis include hypoventilation that is a
consequence of the low H+ concentration. It is often accompanied by mental
confusion and eventually coma. Patients may also suffer from paresthesia.
Other effects of metabolic acidosis include tetany and muscle cramps that
arise due to a decrease in the concentration of unbound Ca2+ in the plasma
(Chapter 8) arising from the alkalosis. Metabolic alkalosis is usually managed
by treating its underlying cause.
Respiratory Acid–Base Disorders
In respiratory acid–base disorders, the primary disturbance is caused by a
change in the partial pressure of arterial CO 2. Respiratory disorders are related
to a defect in the rate of ventilation of lungs or the exchange of gases across the
alveolar membrane. The changes in PCO 2 (Box 9.1) alter the concentrations of
carbonic acid in the blood, which, in turn, dissociates to HCO 3 – and H+.
Some causes of respiratory acidosis are shown in Table 9.2. In general,
obstruction of the airways by disease, or inhibition of the respiratory center in
the brain by disease, trauma or drugs can cause respiratory acidosis.
Respiratory acidosis may be acute or chronic. Acute conditions occur
within minutes or hours. It is usually the low PO 2 (hypoxemia) that is more
dangerous than the high PCO 2 (hypercapnia). Further, renal compensation is
slow, taking two or three days to become effective, so respiratory acidosis is
usually uncompensated. Alveolar hypoventilation is usually the most common
reason for acute respiratory acidosis. Hypoventilation increases the arterial
PCO 2 and so the concentration of H+ also rises quickly. The high PCO 2 and
associated low PO 2 can cause coma and eventually death if untreated. Causes
of acute respiratory acidosis include choking, bronchopneumonia and acute
exacerbation of asthma.
TYPES OF ACID–BASE DISORDERSCZhhVg6]bZY!BVjgZZc9Vlhdc!8]g^hHb^i]:YLddY '(&
Figure 9.8 Computer generated model of
aldosterone.